Lead (Pb) causes nephropathy and hypertension at high body burdens. Blood lead (BPb) concentrations less than 40 ug/dL due to unusual environmental exposure have been considered non- toxic, but clinical experiments indicate Pb may paly a role in the development of renal dysfunction in hypertensive individuals. Our goals are to confirm, expand and delineate these relationships. To accomplish this, subjects with hypertension who subsequently developed nephropathy will be chelated with CaNa2EDTA in a standardized protocol used in previous experiments to estimate body burdens of Pb. These subjects will be compared to controls with renal disease of known cause who have secondary hypertension. Neither group will have past unusual exposure to Pb and will otherwise be similar for BPb and free erythrocyte protoporphyrins. If greater Pb is excreted in the hypertensive nephropathy group, this will support the hypothesis concerning Pb's role. A second study of similar hypertensive nephropathy subjects will evaluate treatment with an oral, efficacious, non- toxic Pb chelator, dimercaptosuccinic acid (DMSA). If improvements in renal function or blood pressure occur with increased urinary excretion of Pb, then the role of Pb will be substantiated in this pathology. Also, bone activity may effect the chelatability of Pb. Hyperparathyroid subjects will be chelated with CaNa2EDTA. Urinary Pb excretion may be higher in these subjects before parathyroidectomy as compared to afterwards. Bone activity may determine how quickly Pb reequilibrates after chelation. Therefore, during this study multiple BPb determinations will allow determination of reequilibration kinetics as a function of bone activity. Analytic techniques for measuring Pb in blood and urine by graphite furnace atomic absorption and stripping voltametry have been developed and fully validated in our laboratory. Methods have been used clinically and in research for several years and have maintained proficiency in CDC and California state proficiency programs.